Understanding What Are the Effects of Parasympathomimetics?

October 10, 2025 •

4 min read

The parasympathetic nervous system (PNS) is responsible for the body's 'rest and digest' functions, and parasympathomimetics are a class of medications that activate this system by mimicking the effects of the primary neurotransmitter, acetylcholine. Understanding what are the effects of parasympathomimetics is crucial for healthcare professionals and patients alike, as these drugs are used to treat a variety of conditions, from glaucoma to urinary retention.

Quick Summary

Parasympathomimetics, or cholinergic drugs, activate the parasympathetic nervous system by mimicking or increasing acetylcholine. Their effects include stimulating digestion, slowing the heart rate, and constricting pupils. These drugs are used to treat conditions like glaucoma and urinary retention but can cause predictable side effects.

Key Points

Rest and Digest Activation: Parasympathomimetics activate the parasympathetic nervous system, promoting 'rest and digest' functions by mimicking or increasing acetylcholine's effects.
Two Primary Mechanisms: These drugs work either directly by binding to muscarinic receptors (e.g., pilocarpine) or indirectly by inhibiting acetylcholinesterase, which breaks down acetylcholine (e.g., neostigmine).
Widespread Systemic Effects: Their impact affects many organ systems, leading to effects such as slower heart rate (bradycardia), increased digestion (motility), pupil constriction (miosis), and increased glandular secretions (salivation, sweating).
Common Therapeutic Uses: Parasympathomimetics are used to treat conditions like glaucoma (to lower intraocular pressure), urinary retention (to stimulate bladder contraction), and myasthenia gravis (to improve muscle strength).
Predictable Side Effects: Most adverse effects are a direct consequence of overstimulating the parasympathetic system and can include nausea, diarrhea, abdominal cramps, and blurred vision.
Caution is Necessary: Due to potential side effects, these drugs are contraindicated in conditions like severe asthma, COPD, or certain heart conditions where increased parasympathetic tone could be harmful.

The Mechanism Behind Parasympathomimetic Effects

Parasympathomimetic drugs, also known as cholinomimetics or cholinergic agents, exert their effects by either directly or indirectly increasing the activity of acetylcholine (ACh). Acetylcholine is the primary neurotransmitter of the parasympathetic nervous system, released by postganglionic parasympathetic nerve endings.

Direct-Acting Parasympathomimetics

Direct-acting agents are muscarinic receptor agonists. They directly bind to and activate muscarinic acetylcholine receptors, mimicking the physiological effects of ACh. This is like pressing a button on the parasympathetic system directly. Examples include bethanechol, which contracts the bladder, and pilocarpine, which induces miosis (pupil constriction) and is used for glaucoma.

Indirect-Acting Parasympathomimetics

Indirect-acting agents are acetylcholinesterase (AChE) inhibitors. They work by blocking the enzyme acetylcholinesterase, which is responsible for breaking down ACh in the synaptic cleft. By inhibiting this breakdown, these drugs increase the concentration and prolong the action of naturally released ACh. This effectively enhances the effects of the parasympathetic nervous system. Examples include neostigmine, used for myasthenia gravis and postoperative bowel or bladder atonia, and physostigmine, used as an antidote for parasympatholytic poisoning.

Systemic Effects of Parasympathomimetics

The effects of parasympathomimetics are widespread due to the extensive distribution of the parasympathetic nervous system throughout the body. The resulting effects are often described using the acronym 'SLUDGE' for Salivation, Lacrimation, Urination, Diaphoresis, Gastrointestinal distress, and Emesis (vomiting).

Cardiovascular System

Bradycardia: Decreased heart rate due to a reduced firing rate of the sinoatrial node.
Hypotension: Decreased blood pressure due to vasodilation, often mediated by endothelium-derived relaxing factor.
Decreased Atrial Contraction: Reduced strength of contraction in the atria (negative inotropy).

Gastrointestinal System

Increased Motility: Stimulation of gut motility, leading to cramping, nausea, and diarrhea.
Increased Secretions: Increased salivation and gastric secretions.
Relaxation of Sphincters: Easing the passage of material through the digestive tract.

Urinary System

Bladder Contraction: Stimulation of the detrusor muscle, helping to relieve urinary retention.
Urinary Urgency: Increased frequency and urgency of urination.

Ocular System

Miosis: Constriction of the pupil due to contraction of the sphincter pupillae muscle.
Accommodation: Contraction of the ciliary muscle for near vision. This is a key effect used in treating glaucoma to increase aqueous humor outflow.

Respiratory System

Bronchoconstriction: Contraction of the bronchial smooth muscle. This can be dangerous in patients with asthma or COPD.
Increased Secretions: Stimulation of tracheobronchial secretions.

Exocrine Glands

Increased Sweating: Stimulates sweat glands (diaphoresis).
Increased Lacrimation: Stimulates tear production.

Comparing Direct- and Indirect-Acting Parasympathomimetics


Feature	Direct-Acting Parasympathomimetics	Indirect-Acting Parasympathomimetics
Mechanism of Action	Directly binds to and activates muscarinic receptors.	Inhibits the enzyme acetylcholinesterase, increasing synaptic ACh.
Onset of Action	Generally faster onset.	Dependent on the rate of ACh accumulation.
Duration of Action	Varies, but can be shorter depending on metabolism.	Can be longer, as they sustain ACh levels over time.
Selectivity	Can have some selectivity for muscarinic receptor subtypes.	Less selective, as they increase ACh at all cholinergic synapses.
Clinical Uses	Glaucoma, urinary retention, dry mouth (e.g., pilocarpine, bethanechol).	Myasthenia gravis, Alzheimer's disease, neuromuscular blockade reversal (e.g., neostigmine, donepezil).
Examples	Pilocarpine, Bethanechol, Cevimeline.	Neostigmine, Physostigmine, Donepezil.

Clinical Uses of Parasympathomimetics

Despite their widespread effects, parasympathomimetics are strategically used to treat specific conditions:

Glaucoma: Pilocarpine and carbachol cause miosis, which improves the drainage of aqueous humor and decreases intraocular pressure.
Urinary Retention: Bethanechol stimulates the detrusor muscle to promote urination.
Myasthenia Gravis: Indirect agents like pyridostigmine increase ACh at the neuromuscular junction, improving muscle strength.
Alzheimer's Disease: Cholinesterase inhibitors, such as donepezil and rivastigmine, are used to boost ACh levels in the brain to temporarily improve cognitive function.
Xerostomia (Dry Mouth): Cevimeline and pilocarpine are used to increase saliva production, particularly in Sjögren's syndrome.

Side Effects and Contraindications

As the effects of parasympathomimetics are an exaggeration of the natural parasympathetic response, the side effects are often predictable consequences of cholinergic overstimulation. Common adverse effects include nausea, vomiting, diarrhea, abdominal cramps, bradycardia, and increased salivation and sweating.

Due to these effects, these drugs are generally contraindicated or used with extreme caution in patients with conditions that could be worsened by parasympathetic stimulation, such as:

Asthma or chronic obstructive pulmonary disease (COPD), due to bronchoconstriction.
Peptic ulcer disease, due to increased gastric acid secretion.
Certain cardiovascular conditions like bradycardia or heart block.
Angle-closure glaucoma, where miosis could worsen the condition.

Conclusion

Parasympathomimetics are a vital class of medications that modulate the body's 'rest and digest' system by mimicking or enhancing the effects of acetylcholine. Their broad impact on organ systems means they are effective for treating a range of conditions, from glaucoma to urinary retention, by promoting specific physiological responses. However, this same broad action necessitates careful consideration of potential side effects and contraindications, underscoring the importance of precise clinical application. The two distinct mechanisms of direct receptor activation and indirect enzyme inhibition allow for targeted therapeutic strategies, making parasympathomimetics an essential tool in pharmacology.

For more in-depth information, the National Center for Biotechnology Information (NCBI) provides extensive resources on pharmacology: https://www.ncbi.nlm.nih.gov/

Frequently Asked Questions

Direct-acting parasympathomimetics bind directly to and activate muscarinic receptors. Indirect-acting agents, also called cholinesterase inhibitors, prevent the breakdown of acetylcholine, thereby increasing its concentration and duration of action.

Parasympathomimetics cause bradycardia (slowed heart rate) by decreasing the firing rate of the sinoatrial node, and can also lead to hypotension (low blood pressure) due to vasodilation.

Drugs like pilocarpine are used for glaucoma because they cause pupillary constriction (miosis) and contraction of the ciliary muscle, which facilitates the drainage of aqueous humor from the eye and lowers intraocular pressure.

Common side effects are predictable and include nausea, vomiting, diarrhea, abdominal cramps, increased salivation and sweating, urinary urgency, and blurred vision.

Yes, indirect-acting parasympathomimetics (cholinesterase inhibitors) like donepezil are used to treat Alzheimer's disease by boosting acetylcholine levels in the brain to improve cognitive function.

Parasympathomimetics can cause bronchoconstriction (constriction of airways) and increased tracheobronchial secretions, which can worsen symptoms in individuals with asthma or COPD.

The 'rest and digest' phrase refers to the primary functions of the parasympathetic nervous system, which are to conserve energy, slow heart rate, and regulate bodily functions like digestion and urination during times of relaxation.